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Article: Central and peripheral administration of secretin inhibits food intake in mice through the activation of the melanocortin system

TitleCentral and peripheral administration of secretin inhibits food intake in mice through the activation of the melanocortin system
Authors
Keywordsarcuate nucleus
feeding
melanocortin system
proopiomelanocortin
secretin
secretin receptor
Issue Date2011
PublisherNature Publishing Group. The Journal's web site is located at http://www.neuropsychopharmacology.org
Citation
Neuropsychopharmacology, 2011, v. 36 n. 2, p. 459-471 How to Cite?
AbstractSecretin (Sct) is released into the circulation postprandially from the duodenal S-cells. The major functions of Sct originated from the gastrointestinal system are to delay gastric emptying, stimulate fluid secretion from pancreas and liver, and hence optimize the digestion process. In recent years, Sct and its receptor (Sctr) have been identified in discrete nuclei of the hypothalamus, including the paraventricular nucleus (PVN) and the arcuate nucleus (Arc). These nuclei are the primary brain sites that are engaged in regulating body energy homeostasis, thus providing anatomical evidence to support a functional role of Sct in appetite control. In this study, the effect of Sct on feeding behavior was investigated using wild-type (wt), Sct -/-, and secretin receptor-deficient (Sctr -/-) mice. We found that both central and peripheral administration of Sct could induce Fos expression in the PVN and Arc, suggesting the activation of hypothalamic feeding centers by this peptide. Consistent with this notion, Sct was found to increase thyrotropin-releasing hormone and melanocortin-4 receptor (Mc4r) transcripts in the PVN, and augment proopiomelanocortin, but reduces agouti-related protein mRNA expression in the Arc. Injection of Sct was able to suppress food intake in wt mice, but not in Sctr -/- mice, and that this effect was abolished upon pretreatment with SHU9119, an antagonist for Mc4r. In summary, our data suggest for the first time that Sct is an anorectic peptide, and that this function is mediated by the melanocortin system. © 2011 American College of Neuropsychopharmacology. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/136251
ISSN
2015 Impact Factor: 6.399
2015 SCImago Journal Rankings: 3.517
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
HK government RGCGRF 763809
HKU 7566/06
Funding Information:

This work was supported by HK government RGC Grant GRF 763809 and HKU 7566/06 M to BKC Chow.

References

 

DC FieldValueLanguage
dc.contributor.authorCheng, CYYen_HK
dc.contributor.authorChu, JYSen_HK
dc.contributor.authorChow, BKCen_HK
dc.date.accessioned2011-07-27T02:11:41Z-
dc.date.available2011-07-27T02:11:41Z-
dc.date.issued2011en_HK
dc.identifier.citationNeuropsychopharmacology, 2011, v. 36 n. 2, p. 459-471en_HK
dc.identifier.issn0893-133Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/136251-
dc.description.abstractSecretin (Sct) is released into the circulation postprandially from the duodenal S-cells. The major functions of Sct originated from the gastrointestinal system are to delay gastric emptying, stimulate fluid secretion from pancreas and liver, and hence optimize the digestion process. In recent years, Sct and its receptor (Sctr) have been identified in discrete nuclei of the hypothalamus, including the paraventricular nucleus (PVN) and the arcuate nucleus (Arc). These nuclei are the primary brain sites that are engaged in regulating body energy homeostasis, thus providing anatomical evidence to support a functional role of Sct in appetite control. In this study, the effect of Sct on feeding behavior was investigated using wild-type (wt), Sct -/-, and secretin receptor-deficient (Sctr -/-) mice. We found that both central and peripheral administration of Sct could induce Fos expression in the PVN and Arc, suggesting the activation of hypothalamic feeding centers by this peptide. Consistent with this notion, Sct was found to increase thyrotropin-releasing hormone and melanocortin-4 receptor (Mc4r) transcripts in the PVN, and augment proopiomelanocortin, but reduces agouti-related protein mRNA expression in the Arc. Injection of Sct was able to suppress food intake in wt mice, but not in Sctr -/- mice, and that this effect was abolished upon pretreatment with SHU9119, an antagonist for Mc4r. In summary, our data suggest for the first time that Sct is an anorectic peptide, and that this function is mediated by the melanocortin system. © 2011 American College of Neuropsychopharmacology. All rights reserved.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.neuropsychopharmacology.orgen_HK
dc.relation.ispartofNeuropsychopharmacologyen_HK
dc.subjectarcuate nucleusen_HK
dc.subjectfeedingen_HK
dc.subjectmelanocortin systemen_HK
dc.subjectproopiomelanocortinen_HK
dc.subjectsecretinen_HK
dc.subjectsecretin receptoren_HK
dc.subject.meshAppetite Regulation - drug effects - genetics - physiology-
dc.subject.meshFeeding Behavior - physiology - psychology-
dc.subject.meshHypothalamus - cytology - metabolism-
dc.subject.meshReceptors, Gastrointestinal Hormone - deficiency - genetics - physiology-
dc.subject.meshSecretin - administration and dosage - deficiency - physiology-
dc.titleCentral and peripheral administration of secretin inhibits food intake in mice through the activation of the melanocortin systemen_HK
dc.typeArticleen_HK
dc.identifier.emailChu, JYS: hitan@graduate.hku.hken_HK
dc.identifier.emailChow, BKC: bkcc@hku.hken_HK
dc.identifier.authorityChu, JYS=rp00684en_HK
dc.identifier.authorityChow, BKC=rp00681en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1038/npp.2010.178en_HK
dc.identifier.pmid20927047-
dc.identifier.pmcidPMC3055665-
dc.identifier.scopuseid_2-s2.0-78650180262en_HK
dc.identifier.hkuros188271en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78650180262&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume36en_HK
dc.identifier.issue2en_HK
dc.identifier.spage459en_HK
dc.identifier.epage471en_HK
dc.identifier.eissn1470-634X-
dc.identifier.isiWOS:000285292200008-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheng, CYY=35423534900en_HK
dc.identifier.scopusauthoridChu, JYS=34975209300en_HK
dc.identifier.scopusauthoridChow, BKC=7102826193en_HK
dc.identifier.citeulike7969801-

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